Angiogenesis is a fundamental process by which new blood vessels are formed, and vascular endothelial growth factor (VEGF) plays an important role in its orchestration. Deregulation of neovascularization may contribute to pulp pathologies. Objectives: The purpose of this in vitro study was to examine if VEGF is upregulated in dental pulp cells exposed to a bonding agent or to HEMA (hydroxyethyl methacrylate). Methods: Mouse odontoblast-like cells (MDPC-23), Raw Macrophages (Mø), or mouse undifferentiated pulp cells (OD-21) were cultured in triplicate wells with DMEM/10% FBS. After 24 h the cells were exposed to 0, 10, 100 or 1000 nM HEMA. Alternatively, cells were exposed to 0 or 10 µg of Single Bond (SB, 3M) at 3 conditions of polymerization: 0, 10 or 40 s light-curing time. The bonding agent was placed on 0.4 µm pore size polycarbonate inserts. After 24 h, ELISA for mouse VEGF (Quantikine, R&D systems) was performed in conditioned medium. Cell viability was determined using Trypan Blue exclusion. T-test or one-way ANOVA were used for statistical analyses. Results: We found that VEGF was upregulated in Mø exposed to HEMA (p<0.001) and to SB (p<0.001). VEGF was also upregulated in MDPC-23 exposed to HEMA (p<0.001) or SB (p=0.018). In contrast, VEGF expression was not statistically significant different in OD-21 pulp cells exposed to HEMA, or to SB (p>0.05).SB polymerized for 0 or 10 s induced death of nearly 100% of Mø, MDPC-23 and OD-21 after 24 h, and SB polymerized for 40 s induced death of 6%, 25%, and 13% respectively. In contrast, 0-1000 nM HEMA did not affect viability of these cells. Conclusions: These results demonstrate that an adhesive resin or HEMA upregulate expression of VEGF by macrophages and odontoblasts, but not by undifferentiated pulp cells. Supported by Dept. of Cariology, Restorative Sciences, Endodontics.

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